Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC
Suppression of anchorage-independent growth by expression of the ataxia-telangiectasia group D complementing gene, ATDC
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DOI：
10.1016/j.bbrc.2006.07.115
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发表时间：
2006-09-22
影响因子：
3.1
通讯作者：
Miyagawa, Kiyoshi
中科院分区：
文献类型：
--
作者：
Hosoi, Yoshio;Kapp, Leon N.;Miyagawa, Kiyoshi
共济失调-毛细血管扩张症D组互补基因（ATDC）位于11 q23，在包括乳腺癌在内的多种癌症中经常观察到杂合性缺失（洛）。使用基因表达系列分析（SAGE）和DNA微阵列分析已经报道了乳腺癌和前列腺癌中ATDC的低表达。我们以前报道过SV-40转化下调ATDC的表达。在本研究中，我们研究了ATDC在肿瘤发生中的作用。首先，我们研究了ATDC在11种癌细胞系中的表达。在4株肿瘤细胞系中未检测到ATDC转录本，在8株肿瘤细胞系中未检测到ATDC蛋白。我们将ATDC表达载体转染到缺乏ATDC mRNA和蛋白表达的Saos-2和BT-549中。在所有的ATDC转染子中，软琼脂中的集落形成效率被显著抑制。这些结果表明，抑制ATDC表达与恶性表型。(c)2006年爱思唯尔公司All rights reserved.
The ataxia-telangiectasia group D complementing gene, ATDC, is located at 11q23, where loss of heterozygosity (LOH) is frequently observed in many kinds of cancers including breast cancer. Underexpression of ATDC in breast and prostate cancer has been reported using serial analysis of gene expression (SAGE) and DNA microarray analysis. We previously reported that SV-40-transformation down-regulates the expression of ATDC. In the present study, we investigated the roles of ATDC in carcinogenesis. First, we investigated the expression of ATDC in 11 cancer cell lines. No detectable transcript was observed in 4 tumor cell lines, and no ATDC protein was detected in 8 tumor cell lines. We transfected ATDC expression vector into Saos-2 and BT-549 that lacked detectable mRNA and protein expression of ATDC. Colony-forming efficiency in soft agar was significantly suppressed in all of the ATDC transfectants. These results suggest that suppressed ATDC expression is associated with malignant phenotype. (c) 2006 Elsevier Inc. All rights reserved.